lipoteichoic-acid and aminoethyl-isothiourea

lipoteichoic-acid has been researched along with aminoethyl-isothiourea* in 1 studies

Other Studies

1 other study(ies) available for lipoteichoic-acid and aminoethyl-isothiourea

Article	Year
Aminoethyl-isothiourea inhibits leukocyte production of reactive oxygen species and proinflammatory cytokines induced by streptococcal cell wall components in human whole blood. Shock (Augusta, Ga.), 2001, Volume: 15, Issue:6 The incidence of severe invasive disease caused by serogroup A streptococci (GAS) is increasing, and to elucidate the role of streptococcal cell wall components in the inflammatory response, human whole blood was stimulated with lipoteichoic acid (LTA, 0.005-50 microg/mL) and peptidoglycan (10 and 100 microg/ml) from Streptococcus pyogenes. Both stimulants increased dose dependently the leukocyte release of cytokines many thousand fold: tumor necrosis factor alpha (0 to 158,000+/-4,900 pg/mL), interleukin (IL)-1beta (85+/-56 to 31,000+/-4,600 pg/mL), IL-6 (30+/-11 to 34,800+/-15,000 pg/mL), and IL-8 (300+/-150 to 29,000+/-14,000 pg/mL). Intracellular leukocyte levels of reactive oxygen species (ROS) as measured by flow cytometry increased 15-20 fold, from 25 to 400-500 mean fluorescence intensity. Aminoethyl-isothiourea (AE-ITU), a relatively selective inhibitor of the inducible nitric oxide synthase (iNOS) and a ROS scavenger, reduced the cytokine production by 70-100%, and intracellular leukocyte ROS levels by 50-70% (all P < 0.05). The non-selective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) did not affect intracellular ROS levels, but it caused a moderate selective inhibition of IL-8 production. Leukocyte NO production (measured up to 36 h) was not enhanced by LTA, peptidoglycan, inactivated streptococci, or cytokine combinations. The mechanisms for the anti-inflammatory effects of AE-ITU may be through a reduction of intracellular ROS levels, or through a direct effect on signal transduction, whereas NO modulation is an unlikely mechanism. Topics: Cell Survival; Cell Wall; Cytokines; Dose-Response Relationship, Drug; Enzyme Inhibitors; Humans; In Vitro Techniques; Inflammation; Interleukin-1; Interleukin-6; Interleukin-8; Leukocytes; Lipopolysaccharides; NG-Nitroarginine Methyl Ester; Nitrates; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Nitrites; Peptidoglycan; Reactive Oxygen Species; Streptococcus pyogenes; Teichoic Acids; Thiourea; Tumor Necrosis Factor-alpha	2001

Article

Year

Aminoethyl-isothiourea inhibits leukocyte production of reactive oxygen species and proinflammatory cytokines induced by streptococcal cell wall components in human whole blood.

Shock (Augusta, Ga.), 2001, Volume: 15, Issue:6

The incidence of severe invasive disease caused by serogroup A streptococci (GAS) is increasing, and to elucidate the role of streptococcal cell wall components in the inflammatory response, human whole blood was stimulated with lipoteichoic acid (LTA, 0.005-50 microg/mL) and peptidoglycan (10 and 100 microg/ml) from Streptococcus pyogenes. Both stimulants increased dose dependently the leukocyte release of cytokines many thousand fold: tumor necrosis factor alpha (0 to 158,000+/-4,900 pg/mL), interleukin (IL)-1beta (85+/-56 to 31,000+/-4,600 pg/mL), IL-6 (30+/-11 to 34,800+/-15,000 pg/mL), and IL-8 (300+/-150 to 29,000+/-14,000 pg/mL). Intracellular leukocyte levels of reactive oxygen species (ROS) as measured by flow cytometry increased 15-20 fold, from 25 to 400-500 mean fluorescence intensity. Aminoethyl-isothiourea (AE-ITU), a relatively selective inhibitor of the inducible nitric oxide synthase (iNOS) and a ROS scavenger, reduced the cytokine production by 70-100%, and intracellular leukocyte ROS levels by 50-70% (all P < 0.05). The non-selective NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) did not affect intracellular ROS levels, but it caused a moderate selective inhibition of IL-8 production. Leukocyte NO production (measured up to 36 h) was not enhanced by LTA, peptidoglycan, inactivated streptococci, or cytokine combinations. The mechanisms for the anti-inflammatory effects of AE-ITU may be through a reduction of intracellular ROS levels, or through a direct effect on signal transduction, whereas NO modulation is an unlikely mechanism.

Topics: Cell Survival; Cell Wall; Cytokines; Dose-Response Relationship, Drug; Enzyme Inhibitors; Humans; In Vitro Techniques; Inflammation; Interleukin-1; Interleukin-6; Interleukin-8; Leukocytes; Lipopolysaccharides; NG-Nitroarginine Methyl Ester; Nitrates; Nitric Oxide Synthase; Nitric Oxide Synthase Type II; Nitrites; Peptidoglycan; Reactive Oxygen Species; Streptococcus pyogenes; Teichoic Acids; Thiourea; Tumor Necrosis Factor-alpha

2001